The cause of localized bone destruction in periodontal disease is unknown, the mechanisms may be similar to those in other conditions where chronic inflammatory cells accumulate adjacent to bone. Among the possible mediators of localized bone destruction in periodontal disease is the lymphokine Osteoclast Activating Factor (OAF). It is the purpose of this study to examine the molecular events which are involved in the production of osteoclast activating factor by chronic inflammatory cells. Specifically, we will use recombinant DNA technology to clone structural gene sequences that code for OAF and examine factors that regulate the expression of this gene in normal and abnormal states. We plan to clone OAF-cDNA and label it to high specific activity so that it can be used as a hybridization probe to conduct a number of biological investigations including: 1) monitoring the amount of OAF mRNA present in lymphocytes obtained from normal subjects and in cells obtained from gingival tissue of patients with periodontal disease, 2) correlating the time course of OAF mRNA production with a time course of bone destruction, and 3) examining the effects of indomethacin and aspirin on OAF mRNA production, since prostaglandins are necessary for the release of OAF by activated lymphocytes and block prostaglandin synthesis.